Na-K-Cl cotransporter contributes to glutamate-mediated excitotoxicity

Journal of Neuroscience

Volumn 23, Issue 12, 2003, Pages 5061-5068

  Beck, Joe ^a   Lenart, Brett ^a   Kintner, Douglas B ^a   Sun, Dandan ^a  

^a UNIVERSITY OF WISCONSIN SCHOOL OF MEDICINE AND PUBLIC HEALTH   (United States)

Author keywords

Active Cl transport; Bumetanide; Cell volume; Excitotoxicity; Na+ entry; Necrosis

Indexed keywords

BUMETANIDE; CHLORIDE ION; CHLORINE; COTRANSPORTER; CYCLOHEXIMIDE; DIZOCILPINE; GLUCOSE; GLUTAMIC ACID; ISOPROTEIN; N METHYL DEXTRO ASPARTIC ACID RECEPTOR; OXYGEN; POTASSIUM; SODIUM; SODIUM ION;

AMINO ACID TRANSPORT; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BRAIN ISCHEMIA; CATION TRANSPORT; CELL DEATH; CHLORIDE TRANSPORT; CONTROLLED STUDY; HOMEOSTASIS; HUMAN; IN VITRO STUDY; INCUBATION TIME; INTRACELLULAR TRANSPORT; MEMBRANE TRANSPORT; NEUROPROTECTION; NEUROTOXICITY; NONHUMAN; POTASSIUM TRANSPORT; PRIORITY JOURNAL; PROTEIN ANALYSIS; PROTEIN SYNTHESIS INHIBITION; RAT; RECEPTOR DOWN REGULATION; REOXYGENATION; SODIUM TRANSPORT;

EID: 0038113310     PISSN: 02706474     EISSN: None     Source Type: Journal    
DOI: 10.1523/jneurosci.23-12-05061.2003     Document Type: Article

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